Incidence and diagnostic significance of minor pathologic changes in the adult pancreas at autopsy:

Stamm, Bernhard

doi:10.1016/s0046-8177(84)80294-4

Cited by 179 publications

(121 citation statements)

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“…Since then, many studies have shown an association between pancreatic adenocarcinoma and intraductal neoplasia (6,7,9). PanIN has been estimated to occur commonly in patients without a history of pancreatic cancer in autopsy samples and in pancreatic tissue removed for nonneoplastic disease, with different studies having a prevalence of around 20 to 30%, though it is considerably more frequent in patients with carcinoma (6,7,8,21). High-grade PanIN occurs only rarely in patients without a history of pancreatic neoplasia (6,7).…”

Section: Discussionmentioning

confidence: 99%

“…Recently, because of the unknown neoplastic potential of flat and papillary epithelial hyperplasia and the poor reproducibility among pathologists in separating papillary hyperplasia with atypia and carcinoma in situ, a new grading system was proposed: LG PanIN (flat and papillary epithelial hyperplasia) and HG PanIN (papillary hyperplasia with atypia and carcinoma in situ; 10 -12). These terms are equivalent to LG and HG pancreatic ductal dysplasia and are thought to separate the lesions into those with a low probability for neoplastic progression (LG PanIN) and a high probability for progression (HG PanIN;11,12,21), though this grading scheme is not yet widely accepted.…”

Section: Discussionmentioning

confidence: 99%

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Neoplasms of the Ampulla of Vater with Concurrent Pancreatic Intraductal Neoplasia: A Histological and Molecular Study

et al. 2001

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Adenoma and adenocarcinoma of the ampulla of Vater are uncommon neoplasms of the gastrointestinal tract that are found with increased frequency in familial adenomatous polyposis syndrome (1-3). Ampullary adenoma represents the precursor lesion to adenocarcinoma, and a coexistent adenoma can be identified frequently in patients with ampullary adenocarcinoma (1, 2). Because of their premalignant nature, ampullary adenomas are often resected either by polypectomy or, in the case of larger lesions, by pancreaticoduodenectomy (1,4,5). An association between adenomas of the ampullary region and pancreatic intraductal neoplasia has not been documented previously. Adenocarcinoma of the pancreas is often associated with pancreatic intraductal neoplasia (PanIN), which is thought to represent the precursor lesion for this cancer (6 -12). Several case reports documenting progression of high-grade (HG) PanIN to invasive pancreatic adenocarcinoma over time (17 mo to 29 y) support the role of PanIN as a precursor of carcinoma (10,13,14).The relationship between ampullary adenoma and PanIN has not been investigated previously, and only one analysis of the relationship between

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neoplasms of the Ampulla of Vater with Concurrent Pancreatic Intraductal Neoplasia: A Histological and Molecular Study

et al. 2001

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“…Unlike the liver, the pancreas cannot be conveniently studied by percutaneous biopsy and is obscured by bowel gas under abdominal ultrasonography. Autopsy series are limited by pancreatic autolysis soon aft er death ( 19 ). In recent years, the development of fat-water magnetic resonance imaging (MRI) has enabled noninvasive assessment of fat and water content in tissues ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

Fatty Pancreas, Insulin Resistance, and β-Cell Function: A Population Study Using Fat-Water Magnetic Resonance Imaging

Wong

Yeung

et al. 2014

American Journal of Gastroenterology

214

181

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OBJECTIVES:Nonalcoholic fatty liver disease is the most common chronic liver disease. Fatty pancreas has also been described but is diffi cult to assess. It is now possible to measure pancreatic and liver fat accurately with magnetic resonance imaging (MRI). We aimed to defi ne the normal range of pancreatic fat and identify factors associated with fatty pancreas. In addition, the effect of fatty liver and fatty pancreas on insulin resistance (IR) and pancreatic ␤ -cell function was studied. METHODS:Fat-water MRI and proton-magnetic resonance spectroscopy were performed on 685 healthy volunteers from the general population to measure pancreatic and liver fat, respectively. On the basis of fasting plasma glucose and insulin levels, the IR and ␤ -cell function were assessed using the homeostasis model assessment (HOMA). RESULTS:Among subjects without signifi cant alcohol consumption or any component of metabolic syndrome, 90 % had pancreatic fat between 1.8 and 10.4 % . Using the upper limit of normal of 10.4 % , 110 (16.1 % ; 95 % confi dence interval 13.3 -18.8 % ) subjects had fatty pancreas. On multivariable analysis, high serum ferritin, central obesity, and hypertriglyceridemia were independent factors associated with fatty pancreas. Subjects with both fatty pancreas and fatty liver had higher HOMA-IR than did those with either condition alone. Fatty pancreas was not associated with HOMA-β after adjusting for liver fat and body mass index.CONCLUSIONS: In all, 16.1 % of this community cohort of adult Hong Kong Chinese volunteers had a fatty pancreas by our defi nition. Central obesity, hypertriglyceridemia, and hyperferritinemia are associated with fatty pancreas. Individuals with fatty pancreas have increased IR.

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“…␤-Cells, which are central in the development of diabetes, constitute the major part of the islets (1). There are reports in diabetic subjects of pathological changes involving not only the islets but the entire pancreatic gland, such as pancreatic volume reduction (2)(3)(4)(5)(6)(7)(8) and lipomatosis (fatty infiltration) of the pancreas (9,10). The lipomatosis reported in autopsy studies has been described as patchy intralobular or perilobular areas of fat replacement of pancreatic parenchyma (9,10).…”

mentioning

confidence: 99%

“…There are reports in diabetic subjects of pathological changes involving not only the islets but the entire pancreatic gland, such as pancreatic volume reduction (2)(3)(4)(5)(6)(7)(8) and lipomatosis (fatty infiltration) of the pancreas (9,10). The lipomatosis reported in autopsy studies has been described as patchy intralobular or perilobular areas of fat replacement of pancreatic parenchyma (9,10). Pancreatic size reduction and lipomatosis have been discussed as possible secondary events involved in atrophy and lipomatosis related to diabetes due to a reduced insulinotropic effect on the acinar cells (11)(12)(13).…”

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confidence: 99%

Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase

et al. 2007

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Both pancreatic volume reduction and lipomatosis have been observed in subjects with diabetes. The underlying molecular and pathological mechanisms are, however, poorly known, and it has been speculated that both features are secondary to diabetes. We have recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and exocrine pancreatic dysfunction caused by heterozygous carboxyl-ester lipase (CEL) mutations. To explore the early pathological events in this syndrome, we performed radiological examinations of the pancreas in nondiabetic mutation carriers with signs of exocrine dysfunction. In a case series study at a tertiary hospital, we evaluated 11 nondiabetic and mutation-positive children with fecal elastase deficiency and 11 age-and sex-matched control subjects using ultrasound and magnetic resonance imaging (MRI) to estimate pancreatic fat content. The pancreata of nondiabetic mutation carriers exhibited increased reflectivity on ultrasound and had MRI findings indicative of lipomatosis. Apparently, carriers of heterozygous CEL mutations accumulate fat in their pancreas before the anticipated development of diabetes. Our findings suggest that lipomatosis of the pancreas reflects early events involved in the pathogenesis of diabetes and exocrine pancreatic dysfunction syndrome. Diabetes 56: 444 -449, 2007 T he pancreas consists of acinar and ductal cells with the islets of Langerhans scattered within the exocrine tissue. ␤-Cells, which are central in the development of diabetes, constitute the major part of the islets (1). There are reports in diabetic subjects of pathological changes involving not only the islets but the entire pancreatic gland, such as pancreatic volume reduction (2-8) and lipomatosis (fatty infiltration) of the pancreas (9,10). The lipomatosis reported in autopsy studies has been described as patchy intralobular or perilobular areas of fat replacement of pancreatic parenchyma (9,10). Pancreatic size reduction and lipomatosis have been discussed as possible secondary events involved in atrophy and lipomatosis related to diabetes due to a reduced insulinotropic effect on the acinar cells (11-13). The underlying molecular and pathophysiological mechanisms are, however, poorly known. Monogenic pancreatic diseases could cast important light on early pathological events and provide the opportunity to study subjects before the development of diabetes.We recently described pancreatic atrophy and lipomatosis in diabetic subjects of two Norwegian families with a novel syndrome of diabetes and pancreatic exocrine dysfunction (MODY8; OMIM [Online Mendelian Inheritance in Man] no. 609812) caused by heterozygous carboxyl-ester lipase (CEL) mutations (14). In that report, computerized tomography of the pancreas was performed in adult mutation carriers, and most of the studied subjects were already diabetic. We hypothesized that the morphologic abnormalities of the pancreas that were identified, particularly the lipomatosis,...

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Incidence and diagnostic significance of minor pathologic changes in the adult pancreas at autopsy:

Cited by 179 publications

References 10 publications

Neoplasms of the Ampulla of Vater with Concurrent Pancreatic Intraductal Neoplasia: A Histological and Molecular Study

Neoplasms of the Ampulla of Vater with Concurrent Pancreatic Intraductal Neoplasia: A Histological and Molecular Study

Fatty Pancreas, Insulin Resistance, and β-Cell Function: A Population Study Using Fat-Water Magnetic Resonance Imaging

Pancreatic Lipomatosis Is a Structural Marker in Nondiabetic Children With Mutations in Carboxyl-Ester Lipase

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